The drug-induced generation of reactive forms of oxygen (superoxide anion, hydroxyl radical and singlet oxygen) can contribute to drug cytotoxicity through attack of reactive oxygen species on intracellular targets (nucleic acids, lipids, proteins) and/or through reactive oxygen-mediate activation of the drug to a reactive intermediate. There are an increasing number of reports describing the pulmonary toxicity of antineoplastic agents. Reactive forms of oxygen have been implicated in the action of several of these agents. The present projects were designed to evaluate this hypothesis in order to better understand the possible biochemical and molecular mechanisms which contribute to this pulmonary toxicity.